LNP023 (20-180 mg/kg; oral administration) prevents KRN (150 μL)-induced arthritis in mice. It is efficacious when administered prophylactically or therapeutically in an experimental model of membranous nephropathy in rats ^[2].

LNP023 demonstrates moderate half-lives (T1/2; Wistar Han rats: 3.4 h, beagle dogs: 5.5 h) and Cmax values (Wistar Han rats: 410 nM, beagle dogs: 2200 nM) after oral dosing (rats: 30 mg/kg, dogs: 10 mg/kg)^[3].

LNP023 shows terminal elimination half-lives (T1/2; Wistar Han rats: 7 h, beagle dogs: 5.6 h) resulting from high plasma clearance rates (8 mL/min/kg for rats and 2 mL/min/kg for dogs) and substantial volumes of distribution (2.3 L/kg for rats and 0.6 L/kg for dogs) after intravenous administration (rats: 1.0 mg/kg, dogs: 0.1 mg/kg)^[3].

LNP023 exhibits potent inhibition of membrane attack complex (MAC) formation induced by the alternative complement pathway (AP) in 50% human serum, with an IC50 value of 130 nM ^[2].

LNP023 demonstrates outstanding selectivity compared to other proteases, with IC50 values exceeding 30 μM across a panel of 41 human proteases, including the AP protein factor D (>100 μM) ^[3].